ANALYSIS OF V-BETA-8.2 CDR3 SEQUENCES FROM SPINAL-CORD T-CELLS OF LEWIS RATS VACCINATED OR TREATED WITH TCR V-BETA-8.2-39-59 PEPTIDE

Experimental autoimmune encephalomyelitis (EAE) in the Lewis rat can b e induced with the administration of Gp-BP. This disease appears to be mediated at least in part by V beta 8.2(+)CD4(+) T cells, which speci fically recognize the BP72-89 encephalitogenic peptide. Treatment or p rotection with V beta 8.2 CDR2 39-59 peptide can suppress or prevent c linical signs of EAE, presumably through the activation of regulatory T cells. interestingly, V beta 8.2(+) T cells continue to persist in t he spinal cord of protected animals, although their appearance in the central nervous system (CNS) is delayed when compared with control ani mals with EAE. As part of our effort to elucidate the mechanism(s) of peptide protection and therapy, we sought to determine whether the V b eta 8.2(+) T cells in the spinal cord of protected or treated rats wer e truly representative of those found in rats with clinical EAE. There fore, we examined the following CNS samples for the Asp(96)Ser(97) mot if, which has been identified previously in V beta 8.2(+) BP-specific, encephalitosenic T cell clones: 1) rats protected with V beta 8.2-39- 59 peptide, 2) rats treated with V beta 8.2-39-59 peptide, and 3) cont rol rats with EAE. Our findings indicate that EAE-associated V beta 8. 2(+) sequences can still be found in both peptide-treated and peptide- protected rats. It appears that administration of V beta 8.2 CDR2 pept ide does not prevent EAE-associated V beta 8.2(+) T cells from infiltr ating the CNS and that other mechanisms are at work to prevent the dev elopment of EAE.